Expansion and Evolution of the X-Linked Testis Specific Multigene Families in the melanogaster Species Subgroup

The testis specific X-linked genes whose evolution is traced here in the melanogaster species subgroup are thought to undergo fast rate of diversification. The CK2ßtes and NACβtes gene families encode the diverged regulatory β-subunits of protein kinase CK2 and the homologs of β-subunit of nascent peptide associated complex, respectively. We annotated the CK2βtes-like genes related to CK2ßtes family in the D. simulans and D. sechellia genomes. The ancestor CK2βtes-like genes preserved in D. simulans and D. sechellia are considered to be intermediates in the emergence of the D. melanogaster specific Stellate genes related to the CK2ßtes family. The CK2ßtes-like genes are more similar to the unique autosomal CK2ßtes gene than to Stellates, taking into account their peculiarities of polymorphism. The formation of a variant the CK2ßtes gene Stellate in D. melanogaster as a result of illegitimate recombination between a NACßtes promoter and a distinct polymorphic variant of CK2ßtes-like ancestor copy was traced. We found a close nonrandom proximity between the dispersed defective copies of DINE-1 transposons, the members of Helitron family, and the CK2βtes and NACβtes genes, suggesting an involvement of DINE-1 elements in duplication and amplification of these genes

Recombination between the ancestor <i>CK2βtes</i>-<i>like</i> gene (GD15860 or GM17570) and <i>NACβtes</i> promoter region.

<p>Signature sequence of putative <i>CK2βtes</i>-like partner is designated in bold italics. The distances in nucleotides from the start of signature sequence and ORF start are indicated in brackets. Broken line shows the site of fusion of the <i>CK2βtes</i>-like and <i>NACβtes</i> sequences as a result of recombination. The tree represents the similarity of the nucleotide sequences in the selected box measured as the number of base differences <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0037738#pone.0037738-S1" target="_blank">[42]</a> and was constructed using the UPGMA method <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0037738#pone.0037738-Sneath1" target="_blank">[43]</a>. The percentage of replicate trees in which the associated sequence clustered together in the bootstrap test (500 iterations) are shown next to the branches. Branches corresponding to partitions reproduced in less than 50% bootstrap replicates are collapsed.</p

Multiple alignment of <i>DINE-1</i>copies in syntenic regions of <i>D. melanogaster</i> and <i>D. simulans/D. sechellia</i>.

<p>(<b>A</b>) Alignment of known and novel <i>DINE-1</i> copies with <i>D. melanogaster DINE-1</i> consensus sequence (DINEYang) <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0037738#pone.0037738-Yang2" target="_blank">[26]</a>; consensus regions are designated according to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0037738#pone.0037738-Yang2" target="_blank">[26]</a>; (<b>B</b>) Alignment of the <i>simINE_ben</i> and <i>DNAREP1_DM</i> consensus sequence <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0037738#pone.0037738-Kapitonov3" target="_blank">[36]</a>.</p

Fate of multigene families in the course of the divergence of <i>melanogaster</i> group species.

<p>Fate of multigene families in the course of the divergence of <i>melanogaster</i> group species.</p

Transcription of the 1.688 Satellite DNA Family Is Under the Control of RNA Interference Machinery in Drosophila melanogaster Ovaries

Here we show that RNA interference (RNAi) machinery operates in Drosophila melanogaster 1.688 satellite transcription. Mutation in the spn-E gene, known to be involved in RNAi in the oocytes, causes an increase of satellite transcript abundance. Transcripts of both strands of 1.688 satellite repeats in germinal tissues were detected. The strength of the effects of the spn-E mutation differs for 1.688 satellite DNA subfamilies and is more pronounced for autosomal pericentromeric satellites compared to the X-linked centromeric ones. The spn-E1 mutation causes an increase of the H3-AcK9 mark and TAF1 (a component of the polymerase II transcriptional complex) occupancy in the chromatin of autosomal pericentromeric repeats. Thus, we revealed that RNAi operates in ovaries to maintain the silenced state of centromeric and pericentromeric 1.688 repeats

Retinoic acid co-treatment aggravates severity of dioxin-induced skin lesions in hairless mice via induction of inflammatory response

Exposure to toxic halogenated polyaromatic hydrocarbons, of which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most potent, induces diverse skin pathologies in humans, including chloracne, hyperkeratosis, hamartomas, etc. While the toxic effects of TCDD have been extensively studied, effective approaches to their treatment are still lacking. Retinoids are commonly used in therapy of acneiform skin diseases. In vitro, retinoids elicit antagonistic effects on keratinocyte differentiation and proliferation, as compared to TCDD, suggesting their potential in treatment of TCDD-induced skin lesions. Nevertheless, the modulation of TCDD activity in skin by retinoids in vivo was never reported. We have used N-TERT keratinocyte cell line and hairless (hr) mice to determine if retinoic acid (RA) can lessen or reverse TCDD-induced effects in vitro and in vivo. RA co-treatment suppressed TCDD-induced changes in the expression of differentiation-associated genes and N-TERT keratinocyte viability in vitro. However, in hairless mice (in vivo), RA/TCDD co-treatment produced more severe effects, than treatment with either of the two compounds individually. RA/TCDD co-application to mouse skin strongly stimulated keratinocyte proliferation, resulting in dramatic epidermal hyperplasia. It has also led to massive immune cell infiltration into the dermis, and increased mRNA expression of inflammation markers, including IL1β, IL6 and S100A7. Thus, retinoids not only appeared ineffective in treatment of TCDD-induced skin lesions in hairless mice, but also resulted in their exaggeration. These in vivo results question previous cell culture-based claims that RA may reduce TCDD-induced skin effects and caution against the reliance on in vitro data in TCDD toxicology research. •Treatment with retinoic acid (RA) is ineffective for dioxin-induced skin lesions in mice.•Co-treatment with dioxin and RA results in psoriasis-like phenotype not seen under treatment with either compound alone.•Strong inflammation is the most prominent effect induced by combined treatment with dioxin and RA